Impact of ligustrazine on chondrocyte apoptosis in knee osteoarthritis through FAK/PI3K/Akt pathway

Authors

  • GUANYUN SHENG Department of Orthopaedics, Liuzhou Traditional Chinese Medical Hospital, Liuzhou City, Guangxi Province, 545001, China Author
  • JING YANG Department of Intensive Care Unit, Liuzhou Traditional Chinese Medical Hospital, Liuzhou City, Guangxi Province, 545001, China Author
  • PENG RONG Guangxi University of Chinese Medicine, graduate school, Nanning City, Guangxi Province, 530000, China Author
  • XUEYI YANG Department of Orthopaedics, Liuzhou Traditional Chinese Medical Hospital, Liuzhou City, Guangxi Province, 545001, China Author

DOI:

https://doi.org/10.25083/rbl/27.3/3559.3569

Keywords:

Ligustrazine, FAK/PI3K/Akt pathway, knee osteoarthritis, chondrocyte apoptosis

Abstract

Objective: To probe into the impact of ligustrazine on chondrocyte apoptosis in knee osteoarthritis (OA) and its pos­sible mechanism.

Methods: Our team extracted the human primary chondrocytes to construct the IL-113-induced chondrocyte damage model, detected the impact of ligustrazine on chondrocyte apoptosis through TUNEL and Western blot, applied Western blot to detect the impact of ligustrazine on matrix-degrading enzymes, matrix-associated proteins, as well as FAK/PI3K/ Akt pathway, using ELISA detected the impact of ligustrazine on MCP-1, IL8, PEG2 and NO levels, applied FAK/PI3K/ Akt pathway inhibitor PF573228 to inhibit FAK/PI3K/Akt pathway to detect whether the chondroprotective impact of ligustrazine was inhibited, constructed a New Zealand rabbit osteoarthritis model, applied HE staining to evaluate the impacts of ligustrazine and ligustrazine+PF573228 on cartilage histomorphology, and applied Western blot to detect the impacts of ligustrazine and ligustrazine+PF573228 on apoptotic proteins, matrix-degrading enzymes and matrix-related proteins in cartilage tissue.

Results: Ligustrazine signally inhibited IL-113-induced chondrocyte apoptosis, reduced Bax, caspase-9, caspase-3, caspase-7, MMP3, MMP13, collagen X protein expression levels, and reduced MCP-1, IL8, PEG2, and MCP-1. NO contents, promoted collagen II and aggrecan protein expression. Additionally, ligustrazine activated the FAK/PI3K/ Akt pathway, and applying PF573228 to inhibit the FAK/PI3K/Akt pathway abolished the chondroprotective impact of ligustrazine. At the in vivo level, ligustrazine activated the FAK/PI3K/Akt pathway to inhibit Bax, caspase-9, caspase-3, caspase-7, MMP3, MMP13, collagen X protein expression levels, promoted collagen II and aggrecan protein expression, and improved cartilage histomorphology.

Conclusion: Ligustrazine exerts chondroprotective impact through FAK/PI3K/Akt pathway

Author Biographies

  • GUANYUN SHENG, Department of Orthopaedics, Liuzhou Traditional Chinese Medical Hospital, Liuzhou City, Guangxi Province, 545001, China

    Guangxi University of Chinese Medicine, graduate school, Nanning City, Guangxi Province, 530000, China

  • JING YANG, Department of Intensive Care Unit, Liuzhou Traditional Chinese Medical Hospital, Liuzhou City, Guangxi Province, 545001, China

    Guangxi University of Chinese Medicine, graduate school, Nanning City, Guangxi Province, 530000, China

  • XUEYI YANG, Department of Orthopaedics, Liuzhou Traditional Chinese Medical Hospital, Liuzhou City, Guangxi Province, 545001, China

    Guangxi University of Chinese Medicine, graduate school, Nanning City, Guangxi Province, 530000, China

RBL273-13

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Published

2024-06-03